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Although silicon (Si) is not recognized as an essential element for general higher plants, it has beneficial effects on the growth and production of a wide range of plant species. Si is known to effectively mitigate various environmental stresses and enhance plant resistance against both fungal and bacterial pathogens. In this review, the effects of Si on plant-pathogen interactions are analyzed, mainly on physical, biochemical, and molecular aspects. In most cases, the Si-induced biochemical/molecular resistance during plant-pathogen interactions were dominated as joint resistance, involving activating defense-related enzymes activates, stimulating antimicrobial compound production, regulating the complex network of signal pathways, and activating of the expression of defense-related genes. The most previous studies described an independent process, however, the whole plant resistances were rarely considered, especially the interaction of different process in higher plants. Si can act as a modulator influencing plant defense responses and interacting with key components of plant stress signaling systems leading to induced resistance. Priming of plant defense responses, alterations in phytohormone homeostasis, and networking by defense signaling components are all potential mechanisms involved in Si-triggered resistance responses. This review summarizes the roles of Si in plant-microbe interactions, evaluates the potential for improving plant resistance by modifying Si fertilizer inputs, and highlights future research concerning the role of Si in agriculture.

Negative motor evoked potentials after cerebral infarction, indicative of poor recovery of limb motor function, tend to be accompanied by changes in fractional anisotropy values and the cerebral pe-duncle area on the affected side, but the characteristics of these changes have not been reported. This study included 57 cases of cerebral infarction whose motor evoked potentials were tested in the 24 hours after the first inspection for diffusion tensor imaging, in which 29 cases were in the negative group and 28 cases in the positive group. Twenty-nine patients with negative motor evoked potentials were divided into two groups according to fractional anisotropy on the affected side of the cerebral peduncle： a fractional anisotropy 〈 0.36 group and a fractional anisotropy 〉 0.36 group. All patients underwent a regular magnetic resonance imaging and a diffusion tensor imaging examina- tion at 1 week, 1, 3, 6 and 12 months after cerebral infarction. The FugI-Meyer scores of their hemiplegic limbs were tested before the magnetic resonance and diffusion tensor imaging exami-nations. In the negative motor evoked potential group, fractional anisotropy in the affected cerebral peduncle declined progressively, which was most obvious in the first 1-3 months after the onset of cerebral infarction. The areas and area asymmetries of the cerebral peduncle on the affected side were significantly decreased at 6 and 12 months after onset. At 12 months after onset, the area asymmetries of the cerebral peduncle on the affected side were lower than the normal lower limit value of 0.83. FugI-Meyer scores in the fractional anisotropy ≥0.36 group were significantly higher than in the fractional anisotropy 〈 0.36 group at 3-12 months after onset. The fractional anisotropy of the cerebral peduncle in the positive motor evoked potential group decreased in the first 1 month after onset, and stayed unchanged from 3-12 months; there was no change in the area of the cerebral peduncle in the first 1-12 months after cerebral infarction. These findings confirmed that if the fractional anisotropy of the cerebral peduncle on the affected side is 〈 0.36 and the area asym-metries 〈 0.83 in patients with negative motor evoked potential after cerebral infarction, then poor hemiplegic limb motor function recovery may occur.

Mitochondrial 3-hydroxy-3-methylglutaryl-coenzyme A synthase 2 (HMGCS2) deficiency is an exceptionally rare autosomal recessive metabolic disorder that impairs ketogenesis. It is typically characterized by hypoketotic hypoglycemia during periods of fasting or metabolic stress. Notably, severe hyperglycemia as an initial presenting symptom has not been previously reported. We report the case of a 6-month-old girl who suddenly developed coma after 1 day of fasting due to repeated vomiting during pneumonia. At presentation, she had hyperglycemia (25.8 mmol/L), ketonuria (1+), glucosuria (3+), metabolic acidosis (pH 6.90), elevated serum alanine transaminase and aspartate aminotransferase levels, increased blood ammonia levels, and liver enlargement on ultrasound. However, fasting insulin, glucagon, and glycated hemoglobin levels were all within the normal range. Whole-exome sequencing identified compound heterozygous mutations in the HMGCS2 gene—c.1175C>T (p.S392L) inherited from the father and c.719A>T (p.A240V) inherited from the mother—thereby confirming the diagnosis of HMGCS2 deficiency. This case highlights severe hyperglycemia as an atypical clinical feature of HMGCS2 deficiency. Increased awareness of such rare manifestations may assist in improving early diagnosis and treatment of this condition.

Mechanical ventilation was frequently conducted in late preterm and term newborn infants because of their severity of neonatal respiratory distress syndrome (NRDS), but the level of positive end expiratory pressure (PEEP) used was not explicit. This study aimed to investigate the efficacy and safety of higher-PEEP in the treatment of NRDS in these infants. Initially, 80 newborn late preterm and term infants diagnosed with NRDS were enrolled, a total of 26 infants were excluded because they were not within the gestational age range of 34 + 0 to 39 + 6 weeks or did not receive mechanical ventilation. Of 54 eligible infants, 6 were excluded: 3 for pre-existing pneumothorax before mechanical ventilation, 1 for hospital transfer, 1 for withdrawal of treatment, and 1 for misdiagnosis with transient tachypnea. Ultimately, 48 infants remained. Following a simple randomization procedure, 23 were assigned to higher-PEEP group and 25 to the control group. The duration of mechanical ventilation was regarded as the primary outcome. We also collected and analyzed data of other clinical factors. We found that higher-PEEP group had significantly shorter durations of mechanical ventilation ( P  = 0.008) and oxygen inhalation ( P  = 0.002) compared to the control. Additionally, the fraction of inspired oxygen (FiO 2 ) ( P  = 0.001) and oxygenation index (OI) ( P  = 0.048) at 24 h after birth were lower in higher-PEEP group compared to the control. Furthermore, higher-PEEP group had a shorter duration of hospitalization ( P  = 0.033). However, no significant differences were observed in the comparisons of complications between the two groups. In summary, higher PEEP could reduce the duration of mechanical ventilation by preserving adequate functional residual capacity, without increasing rates of adverse effects.

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is accepted as an autoimmune disorder of the central nervous system (CNS). NLR family pyrin domain containing 3 (NLRP3) inflammasome, a potent innate inflammatory mediator, can activate IL-1β and induce the migration of T helper cell into CNS. However, the possible role of NLRP3 inflammasome in the pathogenesis of anti-NMDAR encephalitis remains unclear. This study aims to determine the levels of NLRP3 and related cytokines (IL-1β, IL-6, and IL-17) in the cerebrospinal fluid (CSF) of anti-NMDAR encephalitis patients and to assess whether NLRP3 influences the clinical outcomes of this disease. Twenty-five patients with anti-NMDAR encephalitis, 12 viral meningoencephalitis patients and 26 controls with non-inflammatory neurological diseases were recruited. CSF NLRP3 inflammasome, IL-1β, IL-6, and IL-17 were measured by enzyme-linked immunosorbent assay. Thirteen out of 25 patients were re-examed for the concentrations of NLRP3 and cytokines 6 months later. Our results showed significant increases of CSF NLRP3 inflammasome, IL-1β, IL-6, and IL-17 in anti-NMDAR encephalitis patients. There were positive correlations between CSF NLRP3 inflammasome and cytokines in anti-NMDAR encephalitis patients. There was also a positive correlation between maximum modified Rankin Scale (mRS) scores and CSF NLRP3 inflammasome in anti-NMDAR encephalitis patients. During follow-up, the decrease of mRS was positively correlated with the decrease of CSF NLRP3 inflammasomes. These results suggested that the level of CSF NLRP3 inflammasome could represent the severity of anti-NMDAR encephalitis and the reduction of CSF NLRP3 inflammasome could act as an indicator for the prognosis of this disease.

Rheumatoid arthritis (RA) is closely associated with intestinal microbiota dysbiosis, highlighting the therapeutic potential of targeting the microbiota‐gut‐joint axis. Current interventions often overlook the cascade nature of reactive oxygen species (ROS) generation in driving intestinal and systemic inflammation. Herein, a valence‐engineered CeOX‐based nanozyme with self‐cascade catalytic activity is developed, mimicking sequential oxidase‐superoxide dismutase‐peroxidase functions to enable continuous ROS scavenging while minimizing oxygen generation. By precisely tuning Ce3+/Ce4+ ratios from 0.27 to 0.93 through Au deposition (0.23 wt.%→5.2 wt.%), Dual functionality is achieved: 1) enhanced oxygen vacancy generation (71.4%) for efficient ROS scavenging via superoxide anion→hydrogen peroxide→hydroxide ion conversion, and 2) suppressed oxygen production to maintain the anaerobic microenvironment essential for gut microbiota. Encapsulating the nanozyme with sodium alginate (SA) to form Au/CeOX(0.93)@SA ensures resistance to gastric acid upon oral administration. In RA model rats, this strategy restored gut microbial balance, normalized short‐chain fatty acid profiles, and significantly attenuated joint inflammation and cartilage degradation. The therapeutic efficacy is further evidenced by reduced systemic pro‐inflammatory cytokine levels and improved intestinal barrier integrity. This study established a design paradigm for gut microenvironment‐adapted nanozymes, offering a dual‐action strategy for early RA intervention through synchronized ROS elimination and microbiota homeostasis restoration. A valence‐engineered CeOX nanozyme, with its Ce3+/Ce4+ ratio precisely controlled within the range of 0.27 to 0.93 through Au deposition, performs a self‐cascade oxidase‐superoxide dismutase‐peroxidase reaction, enabling continuous reactive oxygen species scavenging while minimizing oxygen generation. Oral sodium alginate‐microencapsulated CeOX nanozyme restores gut microbial homeostasis and exerts dual‐action for early rheumatoid arthritis intervention.

CD138 (also known as syndecan-1) is an important component of endothelial cell glycocalyx, and it is reportedly involved in negative regulation of various inflammatory processes. The clinical implications of circulating and cerebrospinal fluid (CSF) soluble CD138 (sCD138) in patients with Anti- -methyl-d-aspartate receptor (NMDAR) encephalitis remain unclear. The aim of the current study was to investigate associations between serum and CSF sCD138 levels in anti-NMDAR encephalitis patients. The participants enrolled in the study included 27 with anti-NMDAR encephalitis, 11 with viral meningoencephalitis, and 22 controls. At acute stage and 3 to 6-month follow-up time-points, sCD138, tumor necrosis factor-α, matrix metalloproteinase-2, and matrix metalloproteinase-9 in serum and CSF were measured in all participants via enzyme-linked immunosorbent assays. Serum and CSF levels of sCD138 were significantly increased in patients with anti-NMDAR encephalitis. Furthermore, after 3-6 months of follow-up CSF sCD138 levels were significantly decreased in anti-NMDAR encephalitis patients. Changes in sCD138 levels were significantly associated with amelioration of modified Rankin Scale scores in patients with anti-NMDAR encephalitis. In anti-NMDAR encephalitis patients, high circulating, and CSF sCD138 is associated with inflammation and poor clinical prognosis. The present study suggests that sCD138 may be an informative biomarker of inflammation in anti-NMDAR encephalitis.

Anti-N-methyl-D-aspartate receptor (NMDAR) encephalitis is an autoimmune inflammatory brain disease that can develop a variety of neuropsychiatric presentations. However, the underlying nature of its inflammatory neuronal injury remains unclear. Mitochondrial DNA (mtDNA) is recently regarded as a damage-associated molecular pattern molecule (DAMP) that can initiate an inflammatory response. In the presenting study, we aimed to evaluate the levels of cell-free mtDNA in cerebrospinal fluid (CSF) of patients with anti-NMDAR encephalitis and to determine a potential role of cell-free mtDNA in the prognosis of anti-NMDAR encephalitis. A total of 33 patients with NMDAR encephalitis and 17 patients with other non-inflammatory disorders as controls were included in this study. The CSF levels of cell-free mtDNA were measured by quantitative polymerase chain reaction (qPCR). Cytokines including interleukin (IL)-6, IL-10, and tumor necrosis factor alpha (TNF-α) were measured by ELISA. The modified Rankin scale (mRS) score was evaluated for neurologic disabilities. Our data showed that the CSF levels of cell-free mtDNA and inflammation-associated cytokines were significantly higher in the patients with anti-NMDAR encephalitis compared with those in controls. Positive correlations were detected between the CSF levels of cell-free mtDNA and mRS scores of patients with anti-NMDAR encephalitis at both their admission and 6-month follow up. These findings suggest that the CSF level of cell-free mtDNA reflects the underlying neuroinflammatory process in patients with anti-NMDAR encephalitis and correlates with their clinical mRS scores. Therefore, cell-free mtDNA may be a potential prognostic biomarker for anti-NMDAR encephalitis.

There are few proven treatments for acute spontaneous intracerebral haemorrhage, and they all target reducing expansion of the haematoma. The traditional Chinese medicine FYTF-919 (Zhongfeng Xingnao) in an oral solution is comprised of several Chinese herbs that are widely used to treat patients with intracerebral haemorrhage in China on the understanding that they enhance resorption of the haematoma and reduce neuroinflammation. We aimed to provide a reliable assessment of the safety and efficacy of FYTF-919 in patients with moderate to severe acute intracerebral haemorrhage. We did a pragmatic, multicentre, randomised, double-blind, placebo-controlled trial at 26 hospitals in China. We enrolled adults (age ≥18 years) with a diagnosis of symptomatic spontaneous intracerebral haemorrhage (confirmed by brain imaging) within 48 h after the onset of symptoms (or last seen well), which resulted in moderate to severe neurological impairment defined by scores of at least 8 on the National Institute of Health Stroke Scale or between 7 and 14 inclusive on the Glasgow Coma Scale. Randomisation (1:1) was via a central internet-based system with a block grouping method stratified by provincial location of the hospital, severity of neurological impairment, and site of the haematoma in the brain. FYTF-919 and the placebo were masked through consistency in appearance, smell, taste, and other aspects. Participants were allocated to receive 33 mL (or 25 mL via a nasogastric tube if a participant's swallowing was impaired) of either oral liquid FYTF-919 or matching placebo administered at least 30 min after a meal every 8 h (or 6 h via nasogastric tube) over 24 h for 28 days. The primary efficacy outcome was the utility weighted modified Rankin Scale (a seven-level ordinal scale that ranges from 0 [no symptoms] to 6 [death], in which the utility weights of 0·97, 0·88, 0·74, 0·55, 0·20, –0·19, and 0·00 were assigned to the seven levels respectively, with higher scores indicating a better outcome according to the participants' perspective) at 90 days analysed in a general linear model with adjustment for baseline factors. We did several adjusted and sensitivity analyses. Primary analyses were assessed in the intention-to-treat population. This trial is registered at ClinicalTrials.gov, NCT05066620 and is complete. Between Nov 24, 2021, and Dec 28, 2023, of 9000 patients screened, 1648 were randomly assigned to treatment, 817 to the FYTF-919 group and 831 to the placebo group. Before receiving any treatment two patients in the FYTF-919 group and five patients in the placebo group immediately withdrew their consent leaving 1641 participants with available primary outcome data in the intention-to-treat population, 815 in the FYTF-919 group and 826 in the placebo group. 1242 (75·7%) participants consumed 80% or more of the study medication and 994 (60·6%) consumed all of it within 28 days. Mean utility weighted modified Rankin Scale scores at 90 days were 0·44 in the FYTF-919 group and 0·44 in the placebo group (difference 0·01, 95% CI −0·02 to 0·04; p=0·63). The neutral result was consistent in adjusted and sensitivity analyses. There was no significant difference in serious adverse events. This large, randomised, placebo-controlled, double-blind, clinical trial showed no effect of the traditional Chinese medicine herbal compound FYTF-919 on functional recovery, survival, and health-related quality of life in patients with moderate to severe intracerebral haemorrhage. The results reaffirm the need for methodologically rigorous, randomised controlled trials to evaluate the effectiveness of existing therapies, including traditional Chinese medicines that are already in widespread use throughout the world. Key-Area Research and Development Program of Guangdong Province.

Wilson’s disease (WD) is a disease of copper metabolism characterized by excessive copper deposition in the body. It is reported abnormal copper metabolism has been associated with cardiovascular disease. BNP and MMP2/9 were biomarkers of congestive heart failure (CHF). There is rare study to explore whether serum concentrations of BNP, MMP2, and or MMP9 are altered in patients with WD. In this study we determine whether serum concentrations of brain natriuretic peptide (BNP) and matrix metalloproteinases (MMP) 2 and 9 are increased in patients with WD. Serum BNP, MMP2 and MMP9 were measured by an ELISA in 34 patients with hepatic WD, in 68 patients with neurological WD, and in 33 healthy controls. We found serum BNP levels were higher in patients with neurological WD than in healthy controls ( p  = 0.033). Serum MMP2 levels were higher in patients with hepatic ( p  = 0.009) and neurologic ( p  = 0.0004) WD than in controls. Serum MMP9 levels were higher in patients with neurologic WD than in patients with hepatic WD ( p  = 0.002) and controls ( p  = 0.00005), and were higher in patients with hepatic WD than in controls ( p  = 0.03). Serum BNP levels were negatively correlated with ceruloplasmin ( p  = 0.017, r  = −0.215), while serum ( p  = 0.019, r  = −0.221) and MMP9 ( p  = 0.011, r  = −0.231) in patients with WD were negatively correlated with ceruloplasmin. BNP, MMP2, and MMP9 may reflect the deposition of copper in the heart.